scholarly journals Polyamines, vascular smooth muscle, and deoxycorticosterone acetate-salt hypertension.

Hypertension ◽  
1991 ◽  
Vol 18 (1) ◽  
pp. 85-92 ◽  
Author(s):  
E E Soltis ◽  
P S Newman ◽  
J W Olson
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Deoxycorticosterone Acetate ◽  
Acetate Salt ◽  
Salt Hypertension

Comparison of the electrical properties of arterial smooth muscle in normotensive rats and rats with deoxycorticosterone acetate-salt-induced hypertension: Possible involvement of (Na+-K+-Cl−) co-transport

1991 ◽  
Vol 81 (1) ◽  
pp. 73-78 ◽  
Author(s):  
J. P. L. Davis ◽  
A. R. Chipperfield ◽  
A. A. Harper
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Sprague Dawley ◽  
Deoxycorticosterone Acetate ◽  
Acetate Salt ◽  
Na Permeability ◽  
K Concentration ◽  
K Permeability

1. Hypertension was induced in male Sprague-Dawley rats by left unilateral nephrectomy and deoxycorticosterone acetate-salt administration. After 5 weeks, arterial systolic blood pressure was significantly elevated in these animals (191.5 ± 6.0 mmHg, mean ± sd, n = 17) compared with age-matched, unoperated control animals (134.0 ± 4.2 mmHg, n = 8, P < 0.001). 2. The membrane potential of femoral artery vascular smooth muscle measured in vitro was −55.1 ± 6.3 mV (mean ± sd, n = 154) for normotensive and −50.8 ± 5.7 mV (n = 82) for hypertensive animals. The difference in membrane potential was significant (P < 0.001). 3. The relationship between the log of the extracellular K+ concentration and membrane potential was nonlinear over the extracellular K+ concentration range 2.5–20 mmol/l, and showed a small positive shift with hypertension. 4. Tenfold reductions in the extracellular concentrations of Na+ or Cl− resulted in a membrane potential hyperpolarization in vascular smooth muscle from normotensive animals (4.9 ± 2.0 mV, n = 13 and 12.1 ± 1.3 mV, mean ± sd, n = 14, respectively). In vascular smooth muscle from hypertensive animals, the hyperpolarization in low-Na+ media was significantly increased to 12.2 ± 2.6 mV (mean ± sd, n = 5), but that in low-Cl− media was unaffected (2.7 ± 1.6 mV, n = 6). 5. The loop diuretic, bumetanide (10 μmol/l), hyperpolarized the membrane potential in vascular smooth muscle from both normotensive and hypertensive rats, but not in low-Na+ or low-Cl− media. This effect was significantly increased in hypertension, from 1.8 ± 0.7 mV (mean ± sd, n = 8) to 4.0 ± 1.0 mV (n = 5). 6. These results suggest that in these cells, K+ permeability ≫ Na+ permeability > Cl− permeabilty, and that the membrane potential is determined principally by the K+ permeability. In deoxycorticosterone acetate-salt hypertension, the membrane potential is depolarized, Na+ permeability is substantially increased, and there appears to be an increase in the activity of the (Na+-K+-Cl−) co-transporter.

Activation of Two Inward Chloride Transport Systems in Rat Femoral Arterial Smooth Muscle in Deoxycorticosterone Acetate/Salt Hypertension

1997 ◽  
Vol 93 (4) ◽  
pp. 295-298 ◽  
Author(s):  
Alexander A. Harper ◽  
Julian P. L. Davis ◽  
Alan R. Chipperfield
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Membrane Potential ◽  
Systolic Blood Pressure ◽  
Chloride Transport ◽  
Transport Systems ◽  
Arterial Smooth Muscle ◽  
Deoxycorticosterone Acetate ◽  
Acetate Salt ◽  
Salt Hypertension

1. Intracellular [Cl−] ([Cl−]i) was measured with ion-selective microelectrodes in rat femoral arterial smooth muscle in normotensive controls and after the induction of deoxycorticosterone acetate/salt hypertension. 2. Linear regression of [Cl−]i and time after the induction of hypertension showed good correlation (r = 0.96) for 5–6 weeks, as [Cl−]i increased from 30 ± 1 mmol/l (mean ± SD, n = 16), to 49 ± 2 mmol/l (n = 9, P < 0.0001). 3. Arterial systolic blood pressure also increased linearly (r = 0.97) for 5–6 weeks as hypertension developed from 122 ± 1 mmHg (n = 20) to 187 ± 7 mmHg (n = 14): there was consequently a linear relationship between [Cl−]i and arterial systolic blood pressure (r = 0.96). 4. The increase in [Cl−]i was partly because Na+−K+−Cl− co-transport activity, estimated from the fall in [Cl−]i caused by bumetanide, was greater in hypertension (18 mmol/l) than in normotension (10 mmol/l). This finding, and the depolarization of the membrane potential in hypertension (−56 ± 3 mV compared with −64 ± 4 mV in normotension; P < 0.0001), confirms previous studies. 5. The increase in [Cl−]i was also partly due to greater activity of an Na+- and HCO3−-independent, acetazolamide-sensitive inward Cl− transport system; thus acetazolamide reduced [Cl−]i by 7 mmol/l in normotension and by 16 mmol/l in hypertension. 6. In Cl−-free media, the membrane potential in normotension (−59 ± 5 mV) was not significantly different from that in hypertension (−60 ± 4 mV). 7. The role of [Cl−]i in the depolarization of the membrane potential in hypertension is discussed.

Kinin-Mediated Antihypertensive Effect of Captopril in Deoxycorticosterone Acetate–Salt Hypertension

Hypertension ◽  
1996 ◽  
Vol 27 (1) ◽  
pp. 85-89 ◽  
Author(s):  
Ke Chen ◽  
Xuewei Zhang ◽  
Earl W. Dunham ◽  
Ben G. Zimmerman
Keyword(s):  
Antihypertensive Effect ◽  
Deoxycorticosterone Acetate ◽  
Acetate Salt ◽  
Salt Hypertension

scholarly journals Angiotensin Type 1a Receptors in the Subfornical Organ Are Required for Deoxycorticosterone Acetate-Salt Hypertension

Hypertension ◽  
2013 ◽  
Vol 61 (3) ◽  
pp. 716-722 ◽  
Author(s):  
Aline M. Hilzendeger ◽  
Martin D. Cassell ◽  
Deborah R. Davis ◽  
Harald M. Stauss ◽  
Allyn L. Mark ◽  
...  
Keyword(s):  
Subfornical Organ ◽  
Deoxycorticosterone Acetate ◽  
Acetate Salt ◽  
Salt Hypertension ◽  
Angiotensin Type

The Vascular Ornithine Decarboxylase/Polyamine System in Deoxycorticosterone Acetate-Salt Hypertension

1994 ◽  
pp. 279-288
Author(s):  
E. E. Soltis ◽  
P. S. Newman ◽  
M. E. Brown ◽  
J. L. Trowbridge ◽  
H. Guo ◽  
...  
Keyword(s):  
Ornithine Decarboxylase ◽  
Deoxycorticosterone Acetate ◽  
Acetate Salt ◽  
Salt Hypertension

Chronic Caffeine Ingest ion Exacerbates 2-Kidney, 1-Clip Hypertension and Ameliorates Deoxycorticosterone Acetate-Salt Hypertension in Rats

Nephron ◽  
1993 ◽  
Vol 65 (4) ◽  
pp. 619-622 ◽  
Author(s):  
Ki Chul Choi ◽  
Jongeun Lee ◽  
Kyoung Hyup Moon ◽  
Kwang Ki Park ◽  
Soo Wan Kim ◽  
...  
Keyword(s):  
Deoxycorticosterone Acetate ◽  
Acetate Salt ◽  
Salt Hypertension ◽  
Chronic Caffeine
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